Definitive study shows no association between ARID1A mutation status and clinical outcome in endometriosis-related ovarian cancers‡.
Date
2022-06-29ICR Author
Author
Khalique, S
Nash, S
Natrajan, R
Type
Journal Article
Metadata
Show full item recordAbstract
The ARID1A tumour suppressor protein is a component of the SWI/SNF chromatin remodelling complex, which is mutated in approximately 20% of all human cancers. ARID1A mutational status is considered to hold prognostic significance in a range of solid malignancies, yet in endometriosis-related ovarian carcinomas there has been a lack of clarity of its prognostic role. Moreover, the relationship between ARID1A status and immune infiltrate is also poorly understood. In a recent issue of The Journal of Pathology, a large comprehensive study by Heinze, Nazeran et al addressed these areas by reviewing 1,623 endometriosis-associated ovarian carcinomas and correlating ARID1A status using standardised immunohistochemistry to infer mutation status, with comprehensive clinicopathological features, mismatch repair status and CD8+ tumour infiltrating lymphocytes. The study definitively showed that ARID1A status does not provide any independent prognostic value in endometriosis-associated ovarian carcinomas. ARID1A loss was, however, shown to be associated with mismatch repair deficiency and increased CD8+ tumour infiltrating lymphocytes in endometrioid ovarian carcinoma, which may be relevant for future studies. © 2022 The Authors. The Journal of Pathology published by John Wiley & Sons Ltd on behalf of The Pathological Society of Great Britain and Ireland.
Collections
Subject
ARID1A
CD8 tumour infiltrating lymphocytes
biomarker
endometriosis-associated ovarian carcinomas
mismatch repair deficiency
Carcinoma, Endometrioid
DNA-Binding Proteins
Endometriosis
Female
Humans
Mutation
Nuclear Proteins
Ovarian Neoplasms
Transcription Factors
Research team
Functional Genomics
Language
eng
Date accepted
2022-05-30
License start date
2022-06-29
Citation
Journal of Pathology, 2022, 258 (1), pp. 1 - 3
Publisher
WILEY